Evaluation of Middle Ear Function by Tympanometry and the Influence of Lower Barometric Pressure at High Altitude

Author(s):  
Tao Jiang ◽  
Liping Zhao ◽  
Yanbo Yin ◽  
Huiqian Yu ◽  
Qingzhong Li
2012 ◽  
Vol 112 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Claire de Bisschop ◽  
Jean-Benoit Martinot ◽  
Gil Leurquin-Sterk ◽  
Vitalie Faoro ◽  
Hervé Guénard ◽  
...  

Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V̇o2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V̇o2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V̇o2 max at sea level ( r = 0.41–0.42, P < 0.1) and more so at altitude ( r = 0.56–0.59, P < 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity.


2015 ◽  
Vol 118 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Andrew M. Luks

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness—acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema—and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management.


Author(s):  
Cynthia M. Beall ◽  
Kingman P. Strohl

Biological anthropologists aim to explain the hows and whys of human biological variation using the concepts of evolution and adaptation. High-altitude environments provide informative natural laboratories with the unique stress of hypobaric hypoxia, which is less than usual oxygen in the ambient air arising from lower barometric pressure. Indigenous populations have adapted biologically to their extreme environment with acclimatization, developmental adaptation, and genetic adaptation. People have used the East African and Tibetan Plateaus above 3,000 m for at least 30,000 years and the Andean Plateau for at least 12,000 years. Ancient DNA shows evidence that the ancestors of modern highlanders have used all three high-altitude areas for at least 3,000 years. It is necessary to examine the differences in biological processes involved in oxygen exchange, transport, and use among these populations. Such an approach compares oxygen delivery traits reported for East African Amhara, Tibetans, and Andean highlanders with one another and with short-term visitors and long-term upward migrants in the early or later stages of acclimatization to hypoxia. Tibetan and Andean highlanders provide most of the data and differ quantitatively in biological characteristics. The best supported difference is the unelevated hemoglobin concentration of Tibetans and Amhara compared with Andean highlanders as well as short- and long-term upward migrants. Moreover, among Tibetans, several features of oxygen transfer and oxygen delivery resemble those of short-term acclimatization, while several features of Andean highlanders resemble the long-term responses. Genes and molecules of the oxygen homeostasis pathways contribute to some of the differences.


1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.


1982 ◽  
Vol 100 (1) ◽  
pp. 147-157
Author(s):  
J B West

Hyperventilation is one of the most important features of acclimatization to high altitude. Resting ventilation at extreme altitudes increases up to fourfold and exercise ventilation for a given work level increases to the same extent. Hypoxic stimulation of the peripheral chemoreceptors is the chief mechanism for the hyperventilation but there is also evidence that central sensitization of the respiratory centres occurs. Permanent residents of high altitude have a blunted hypoxic ventilatory response compared to acclimatized lowlanders. Cardiac output increases in responses to acute hypoxia but returns to normal in acclimatized lowlanders. Oxygen uptake at extreme altitudes is markedly limited by the diffusion properties of the blood gas barrier. As a consequence the maximal oxygen consumption of a climber near the summit of Mount Everest is near his basal oxygen requirements. Maximal oxygen consumption is so sensitive to barometric pressure that it may be that day-to-day variations will affect the chances of a climber reaching the summit without supplementary oxygen.


1985 ◽  
Vol 58 (3) ◽  
pp. 978-988 ◽  
Author(s):  
G. E. Gale ◽  
J. R. Torre-Bueno ◽  
R. E. Moon ◽  
H. A. Saltzman ◽  
P. D. Wagner

To investigate the effects of both exercise and acute exposure to high altitude on ventilation-perfusion (VA/Q) relationships in the lungs, nine young men were studied at rest and at up to three different levels of exercise on a bicycle ergometer. Altitude was simulated in a hypobaric chamber with measurements made at sea level (mean barometric pressure = 755 Torr) and at simulated altitudes of 5,000 (632 Torr), 10,000 (523 Torr), and 15,000 ft (429 Torr). VA/Q distributions were estimated using the multiple inert gas elimination technique. Dispersion of the distributions of blood flow and ventilation were evaluated by both loge standard deviations (derived from the VA/Q 50-compartment lung model) and three new indices of dispersion that are derived directly from inert gas data. Both methods indicated a broadening of the distributions of blood flow and ventilation with increasing exercise at sea level, but the trend was of borderline statistical significance. There was no change in the resting distributions with altitude. However, with exercise at high altitude (10,000 and 15,000 ft) there was a significant increase in dispersion of blood flow (P less than 0.05) which implies an increase in intraregional inhomogeneity that more than counteracts the more uniform topographical distribution that occurs. Since breathing 100% O2 at 15,000 ft abolished the increased dispersion, the greater VA/Q mismatching seen during exercise at altitude may be related to pulmonary hypertension.


1995 ◽  
Vol 78 (6) ◽  
pp. 2279-2285
Author(s):  
G. L. Colice ◽  
Y. J. Lee ◽  
J. Chen ◽  
H. K. Du ◽  
G. Ramirez ◽  
...  

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.


2018 ◽  
Vol 3 (3) ◽  
pp. 203 ◽  
Author(s):  
Anil Gurtoo

<p>Increase in altitude causes decrease in atmospheric barometric pressure that results in decrease of inspired<br />partial pressure of oxygen, a source for stress and pose a challenge to climbers/trekkers or persons posted on<br />high altitude areas. This review discusses about the high altitude sickness, their incidence rates, pathophysiology<br />and the classic model of acclimatisation, which explains about how oxygen requirement in extreme environment<br />is achieved by complex interplay among pulmonary, hematological and cardiovascular processes. The acute<br />high altitude illness (AHAI) is basically composed of two syndromes: cerebral and pulmonary that can afflict<br />un-acclimatised climbers/trekkers. The cerebral syndrome includes acute mountain sickness (AMS) and high<br />altitude cerebral oedema (HACO) and pulmonary syndrome typically refers to high altitude pulmonary oedema<br />(HAPO). The core physiological purpose, according to the classic model is centered upon the optimisation of<br />increased delivery of oxygen to the cells through a coherent response involving increased ventilation, cardiac<br />output and hemoglobin concentration with aim to increase the oxygen flux across the oxygen cascade, which<br />will help in preventing the development of majority of high altitude illness.</p>


1979 ◽  
Vol 65 (3) ◽  
pp. 123-130
Author(s):  
W. D. McNicoll ◽  
S. G. Scanlan

AbstractThe combination of nasal septal deviation and Eustachian tube dysfunction, in the absence of any other pathology, constitutes the Nose-Ear Distress Syndrome. We have undertaken a clinical assessment of the relationship between uncomplicated deviation of the nasal septum and Eustachian tube dysfunction in naval personnel who are serving in environments of primarily increased barometric pressure.One hundred and twenty candidates to the submarine, diving and aircrew branches of the Royal Navy who presented with the nose-ear distress syndrome were initially surveyed. None were able to equilibrate their middle ear pressures at an increased ambient pressure of 3 metres of water. Submucous resection was performed on 116, of whom 110 (94.83%) were able to equilibrate their middle ear pressures at an increased ambient pressure of 9 metres of water post-operatively.Xenon 113 scintigraphy was performed on a further 25 recruits to delineate the post-nasal airflow. This investigation was performed pre- and post-operatively. Pre-operatively, scintigraphy showed the presence of turbulence in the post-nasal space, while post-operatively the turbulence was absent. All the candidates were unable to equilibrate their middle ear pressures pre-operatively, but after submucous resection 24 (96%) were able to equilibrate their middle ear pressures at an increased barometric pressure of 9 metres of water.


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